Ether stress stimulates noradrenaline release in the hypothalamic paraventricular nucleus.

Differential normal-pulse voltammetry was combined with treated carbon fibre electrodes for monitoring in vivo extracellular catechols synthesized by noradrenergic terminals innervating the paraventricular hypothalamic nucleus. From urethane-anaesthetized rats, pretreated with a monoamine oxidase inhibitor, pargyline, we were able to monitor a catechol signal which unequivocally corresponded to extracellular noradrenaline, and we observed that ether inhalation for 2 min induced an immediate increase in this signal. Electrical stimulation of the ventral noradrenergic pathway (10 Hz for 40 s) induced a similar effect. On the other hand, from freely moving rats which were not treated with pargyline, we recorded a catechol peak which mainly corresponded to 3,4-dihydroxyphenylacetic acid which was synthesized by noradrenergic terminals. However, electrochemical and biochemical evidence strongly suggested that the increase in this signal induced by a 2-min ether stress does not correspond to 3,4-dihydroxyphenylacetic acid, but to an increase in the extracellular noradrenaline concentration. In both experimental situations the time course of the effects was identical: ether stress induced an immediate and pronounced increase in norepinephrine release, and this effect lasted as long as the stimulus duration. This effect appeared specific for noradrenergic terminals, since no effect on dopamine release was observed when recorded from the striatum or behind the paraventricular hypothalamic nucleus from the A13 dopaminergic group. In conclusion, our data are consistent with those which suggest a facilitatory action of norepinephrine on neurosecretory neurons whose cell bodies are located in the paraventricular hypothalamic nucleus and which play a major role in the hormonal response to stress.